National cancer screening program discovered many asymptomatic gastric diseases including gastric polyps and early gastric cancer (EGC). Gastric polyps found by esophagogastroduodenoscopy (EGD) are divided into elevated, flat, and depressed lesion by gross morphology. Gastric elevated lesions are originated from gastric epithelial cells and nonepithelial cells. Gastric elevated lesion originated from surface epithelium can be diagnosed by magnifying endoscopy or narrow band imaging, and gastric lesion originated from subepithelial tissue can be diagnosed by endoscopic ultrasonography. Polypoid gastric cancer and the other gastric polyps including benign disease entity will be discussed herein.

Gastric polyps are locally elevated lesion protruding into gastric lumen and incidentally discovered in about 2% of EGD.1 Most patients are asymptomatic, but infrequently, complications such as bleeding or gastric obstruction can be accompanied. Endoscopic appearance is usually salmon pink or red colored and they are sessile, semipedunculated, or pedunculated in shape. Topographically, fundic gland polyp (FGP) usually occurs in the body or fundus and adenoma usually occurs in the antrum. Some polyps such as hyperplastic polyps, FGP, carcinoids, and metastases tend to be multiple lesions. Some polyps tend to have malignant transformation (FGP, adenoma, and carcinoid), while hyperplastic polyps, inflammatory fibrinoid polyps, and hamartomatous polyps are seldom known to have malignant transformation.

Elster10 first described FGP in 1976. Histologically, FGP is composed of cystically dilated glands lined by fundic epithelium (parietal cell, chief cell, admixed with normal glands) and most common gastric polyp. Endoscopically, this polyp is sessile and less than 0.5 cm in mean diameter. FGP appears as glassy, transparent, and of the same color as adjacent normal mucosa. FGP is multiple or single mass and occurs in the fundus or body mucosa which secrete gastric acid. Adjacent mucosa is usually clear without inflammation or H. pylori infection.

FGPs are usually multiple especially associated with familial adenomatous polyposis or Peutz-Jeghers syndrome and may be found in men and women of relatively young age (Fig. 3). The frequent finding of genetic alteration in familial adenomatous polyposis suggests that this polyp is neoplastic rather than hamartomatous origin.11 Recently, one series reported adenocarcinoma arising from FGPs in patients with familial adenomatous polyposis or attenuated familial adenomatous polyposis.12,13 FGPs especially in young age and multiple in number might be associated with familial adenomatous polyposis, and these cases were accompanied by dysplasia in up to 40%.14

Sporadic FGP is usually found in middle aged women with accompanying dysplasia at the incidence of 0% to 5%, but it is not related to malignant transformation. Alteration of the β-catenin gene is found in 91% of patients and these patients have higher risk for colonic polyp, adenoma, and adenocarcinoma compared with control group which has no FGP.15

Recently, FGP is known to be one of the side effects related to proton pump inhibitor. In patients using proton pump inhibitors, there is associated hypertrophy and hyperplasia of parietal cells, and long standing exposure to this drug may increase FGPs by 4-folds compared with control group.16 However, dysplasia related to proton pump inhibitor is still rare and further study will be necessary in the future.

Gastric adenoma is circumscribed, polypoid lesions composed of either tubular and/or villous structures lined by dysplastic epithelium. Adenoma is a precursor lesion of adenocarcinoma. Gastric adenoma is subdivided into low grade dysplasia and high grade dysplasia according to the degree of dysplasia (based on the degree of nuclear crowding, hyperchromasia, stratification, mitotic activity, cytoplasmic differentiation, and architectural distortion). Most gastric adenomas arise in the background of atrophic gastritis with intestinal metaplasia. The incidence of adenoma increases with age and adenocarcinoma arising from adenoma is reported up to 9% to 20%.17 The majority of gastric adenomas are found in the antrum and angle and secondly in the fundus. Endoscopic finding is solitary, exophytic sessile, or pedunculated mass and rarely flattened or slightly depressed lesion. Adenomas have light red color and show papillary configuration. Easy contact bleeding is not a typical finding of gastric adenoma usually measuring up to 3 to 4 cm in diameter. Adenomas of larger size, especially of more than 2 cm in diameter, with red color, central depression, ulcer, and villous configuration are known to have increased risk of carcinomatous transformation. According to one series, 9% of low grade adenomas and 25% of high grade adenomas showed the evidence of malignant transformation.18 Even when endoscopic biopsy reveals adenoma, there might be carcinomatous change in excised specimen, so gastric adenoma should be treated by local excision, usually by endoscopic mucosal resection, and needs to be followed up. In addition, since they may be accompanied by coexistent carcinoma elsewhere in the stomach, thorough endoscopic examination of the whole stomach is warranted.

Gastric carcinoids are well-differentiated endocrine tumors composed of nonfunctioning enterochromaffin-like cells arising in the oxyntic mucosa of the body or fundus.19 Gastric carcinoids account for less than 2% of gastric neoplasm, and represents less than 1% of carcinoids.20 There are three distinct clinical settings: autoimmune atrophic gastritis, patients with concomitant Zollinger-Ellison syndrome and MEN-1 syndrome, and sporadic case.21 In the first two cases, they are usually multiple, broad-based, yellowish, polypoid masses of less than 2 cm in diameter. In the sporadic cases, the tumors are larger and single and similar to carcinoma (bleeding, obstruction, or metastases). Endoscopic ultrasonographic finding is well demarcated, homogenous and hypoechoic submucosal mass. They grow slowly but can metastasize to lymph node or the liver. The size, invasiveness and histologic subtype of mass correlates with the probability of metastasis. Treatment is dependent on the size and histologic subtype. Carcinoids less than 1 to 2 cm in size, less than five in number and confined within the submucosal layer can be treated by endoscopic mucosal resection. Surgical local excision is recommended for carconoids larger than 2 cm in size.

EGC is defined as invasive gastric cancer which invades no more deeply than the submucosa, irrespective of lymph node metastasis. Endoscopically, there are three subtypes of polypoid EGC: elevated (type I), superficial elevated (type IIa), and mixed type (IIa+IIc, etc). Also among advanced gastric cancer (AGC), Bormann type I and II are polypoid gastric cancer.

Various subtypes of gastric polyps with different risks of malignant transformation which are similar with polypoid gastric cancer were revealed in endoscopic procedure. Although benign and malignant gastric polypoid tumor can be revealed in endoscopic procedure, magnifying endoscopy or narrow band imaging, and endoscopic ultrasonography could help their differential diagnosis and therapeutic strategies more easily. Most of all, meticulous endoscopic examination, accurate biopsy for indefinite lesion, reconsidering result with pathologic reports, and periodic follow-up examination are critical.